Seok‐Gu Kang
연세대학교 의과대학 신경외과학교실 · 의학
Seok-Gu Kang 교수의 연구실은 뇌신경종양, 특히 고급 뇌신생물성 종양(Glioblastoma, GBM)의 치료 전략 개발에 초점을 맞추고 있습니다. 특히 종양 미세환경 내 면역조절, 대사 억제, 보조세포(예: Br-MSCs, MSLCs)의 기여 메커니즘을 규명하며 새로운 표적 치료법을 모색하고 있습니다. 면역검사제제와 표준치료제의 조합요법, ROS 조절 및 신호전달 경로(예: PI3K, ERK, p38 MAPK)의 조절을 통해 GBM의 침습성과 치료 저항성을 극복하고자 합니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Our findings suggest that dual inhibition of tumor bioenergetics is a novel and effective strategy for the treatment of GBM.
Our results indicate that cells similar to BM-MSCs exist in the brain. These Br-MSCs appear to be located within the vascular niche and may provide the mesenchymal elements of this niche. Because MSCs may be part of the cellular response to tissue injury, Br-MSCs may represent targets in the therapy of pathological processes such as stroke, trauma, and tumorigenesis.
Insulin exerts an anti-apoptotic activity by suppressing the excessive accumulation of ROS within cells through signaling pathways including stimulation of PI3 kinase and ERK in HepG2 cells.
<b>Background</b>: Although programmed death-1 (PD-1) blockade is effective in treating several types of cancer, the efficacy of this agent in glioblastoma (GBM) is largely unknown. <b>Methods</b>: We evaluated therapeutic effects of anti-PD-1, temozolomide (TMZ), and their combination in an orthotopic murine GBM model. The phenotype, number, and composition of lymphocytes were evaluated using flow cytometry. Transcriptional profiles of tumor tissues were analyzed using microarrays. Generation o
1. MSLCs activate p38 MAPK-ZEB1 signaling in GBM cells through C5a in a paracrine manner, thereby boosting the invasiveness of GBM cells in the tumor microenvironment.2. Neutralizing of C5a could be a potential therapeutic target for GBM by inhibition of mesenchymal phenotype.
